Data gathered suggests that there is a deficit in repair of UV damaged DNA in Systemic Lupus Erythematosus. This project proposes to provide additional clinical and experimental data on this proposal. Further, the problem of genetic and/or virus factors are being investigated by two breeding schemes. These are designed to maximize the difference in anticipated results, so that no ambiguity of results is obtainnd. Resolution of the deficit as enzymatic defect is to be accomplished by somatic cell hybridization (complementation test) and by supplementation. Experiments are to include the usefulness of the assay in detecting repair deficits of amniotic fluid cells and in heterozygote detection.